Database : MEDLINE
Search on : Collagen and Type and I [Words]
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[PMID]: 29511368
[Au] Autor:Fisher A; Fisher L; Srikusalanukul W; Smith PN
[Ad] Address:Department of Geriatric Medicine, The Canberra Hospital, Canberra, ACT Health, Canberra, Australia.
[Ti] Title:Bone Turnover Status: Classification Model and Clinical Implications.
[So] Source:Int J Med Sci;15(4):323-338, 2018.
[Is] ISSN:1449-1907
[Cp] Country of publication:Australia
[La] Language:eng
[Ab] Abstract:To develop a practical model for classification bone turnover status and evaluate its clinical usefulness. Our classification of bone turnover status is based on internationally recommended biomarkers of both bone formation (N-terminal propeptide of type1 procollagen, P1NP) and bone resorption (beta C-terminal cross-linked telopeptide of type I collagen, bCTX), using the cutoffs proposed as therapeutic targets. The relationships between turnover subtypes and clinical characteristic were assessed in1223 hospitalised orthogeriatric patients (846 women, 377 men; mean age 78.1±9.50 years): 451(36.9%) subjects with hip fracture (HF), 396(32.4%) with other non-vertebral (non-HF) fractures (HF) and 376 (30.7%) patients without fractures. Six subtypes of bone turnover status were identified: 1 - normal turnover (P1NP>32 µg/L, bCTX≤0.250 µg/L and P1NP/bCTX>100.0[(median value]); 2- low bone formation (P1NP ≤32 µg/L), normal bone resorption (bCTX≤0.250 µg/L) and P1NP/bCTX>100.0 (subtype2A) or P1NP/bCTX<100.0 (subtype 2B); 3- low bone formation, high bone resorption (bCTX>0.250 µg/L) and P1NP/bCTX<100.0; 4- high bone turnover (both markers elevated ) and P1NP/bCTX>100.0 (subtype 4A) or P1NP/bCTX<100.0 (subtype 4B). Compared to subtypes 1 and 2A, subtype 2B was strongly associated with nonvertebral fractures (odds ratio [OR] 2.0), especially HF (OR 3.2), age>75 years and hyperparathyroidism. Hypoalbuminaemia and not using osteoporotic therapy were two independent indicators common for subtypes 3, 4A and 4B; these three subtypes were associated with in-hospital mortality. Subtype 3 was associated with fractures (OR 1.7, for HF OR 2.4), age>75 years, chronic heart failure (CHF), anaemia, and history of malignancy, and predicted post-operative myocardial injury, high inflammatory response and length of hospital stay (LOS) above10 days. Subtype 4A was associated with chronic kidney disease (CKD), anaemia, history of malignancy and walking aids use and predicted LOS>20 days, but was not discriminative for fractures. Subtype 4B was associated with fractures (OR 2.1, for HF OR 2.5), age>75 years, CKD and indicated risks of myocardial injury, high inflammatory response and LOS>10 days. We proposed a classification model of bone turnover status and demonstrated that in orthogeriatric patients altered subtypes are closely related to presence of nonvertebral fractures, comorbidities and poorer in-hospital outcomes. However, further research is needed to establish optimal cut points of various biomarkers and improve the classification model.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:In-Process
[do] DOI:10.7150/ijms.22747

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[PMID]: 29481955
[Au] Autor:Du T; Niu X; Li Z; Li P; Feng Q; Fan Y
[Ad] Address:Key Laboratory for Biomechanics and Mechanobiology of Ministry of Education, School of Biological Science and Medical Engineering, Beihang University, Beijing 100083, China.
[Ti] Title:Crosslinking induces high mineralization of apatite minerals on collagen fibers.
[So] Source:Int J Biol Macromol;113:450-457, 2018 Feb 23.
[Is] ISSN:1879-0003
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:Type I collagen, as the critical organic component of bone matrix, plays a template role in mineralization. Gamma-ray irradiation is used to prepare collagen with different crosslinking degrees without introducing foreign substances for mineralization. Significant improvement in crosslinking degree of collagen can be inferred by enzymolysis and differential scanning calorimetry analysis. Scanning electron microscopy observation reveals that, as crosslinking degree increases, the pore structure of collagen becomes more compact. Fourier transform infrared spectroscopy analysis shows the intact retention of classical triple-helical structure of collagen after crosslinking and the following mineralization. Atomic force microscopy characterization, calcium and phosphorus assay kit tests and thermogravimetry measurements indicate that the more compact the collagen structure, the more hydroxyapatite can attach on collagen fibers. These findings reveal the high crosslinking degree of collagen is favorable for the improvement of mineralization ability by providing a more stable and compact network structure. Such crosslinked collagen may provide a more potential way for the preparation of bone substitute materials.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  3 / 53429 MEDLINE  
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[PMID]: 29458012
[Au] Autor:DiMario JX
[Ad] Address:Department of Cell Biology and Anatomy, Rosalind Franklin University of Medicine and Science, Chicago Medical School, North Chicago, Illinois. Electronic address: joseph.dimario@rosalindfranklin.edu.
[Ti] Title:KLF10 Gene Expression Modulates Fibrosis in Dystrophic Skeletal Muscle.
[So] Source:Am J Pathol;, 2018 Feb 16.
[Is] ISSN:1525-2191
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Dystrophic skeletal muscle is characterized by fibrotic accumulation of extracellular matrix components that compromise muscle structure, function, and capacity for regeneration. Tissue fibrosis is often initiated and sustained through transforming growth factor-ß (TGF-ß) signaling, and Krüppel-like factor 10 (KLF10) is an immediate early gene that is transcriptionally activated in response to TGF-ß signaling. It encodes a transcriptional regulator that mediates the effects of TGF-ß signaling in a variety of cell types. This report presents results of investigation of the effects of loss of KLF10 gene expression in wild-type and dystrophic (mdx) skeletal muscle. On the basis of RT-PCR, Western blot, and histological analyses of mouse tibialis anterior and diaphragm muscles, collagen type I (Col1a1) and fibronectin gene expression and protein deposition were increased in KLF10 mice, contributing to increased fibrosis. KLF10 mice displayed increased expression of genes encoding SMAD2, SMAD3, and SMAD7, particularly in diaphragm muscle. SMAD4 gene expression was unchanged. Expression of the extracellular matrix remodeling genes, MMP2 and TIMP1, was also increased in KLF10-deficient mouse muscle. Histological analyses and assays of hydroxyproline content indicated that the loss of KLF10 increased fibrosis. Dystrophic KLF10-null mice also had reduced grip strength. The effects of loss of KLF10 gene expression were most pronounced in dystrophic diaphragm muscle, suggesting that KLF10 moderates the fibrotic effects of TGF-ß signaling in chronically damaged regenerating muscle.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

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[PMID]: 29438824
[Au] Autor:Creecy A; Uppuganti S; Unal M; Clay Bunn R; Voziyan P; Nyman JS
[Ad] Address:Department of Biomedical Engineering, Vanderbilt University, Nashville, TN 37232, United States; Department of Orthopaedic Surgery & Rehabilitation, Vanderbilt University Medical Center, Nashville, TN 37232, United States; Center for Bone Biology, Vanderbilt University Medical Center, Nashville,
[Ti] Title:Low bone toughness in the TallyHO model of juvenile type 2 diabetes does not worsen with age.
[So] Source:Bone;110:204-214, 2018 Feb 10.
[Is] ISSN:1873-2763
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Fracture risk increases as type 2 diabetes (T2D) progresses. With the rising incidence of T2D, in particular early-onset T2D, a representative pre-clinical model is needed to study mechanisms for treating or preventing diabetic bone disease. Towards that goal, we hypothesized that fracture resistance of bone from diabetic TallyHO mice decreases as the duration of diabetes increases. Femurs and lumbar vertebrae were harvested from male, TallyHO mice and male, non-diabetic SWR/J mice at 16weeks (n≥12 per strain) and 34weeks (n≥13 per strain) of age. As is characteristic of this model of juvenile T2D, the TallyHO mice were obese and hyperglycemic at an early age (5weeks and 10weeks of age, respectively). The femur mid-shaft of TallyHO mice had higher tissue mineral density and larger cortical area, as determined by micro-computed tomography, compared to the femur mid-shaft of SWR/J mice, irrespective of age. As such, the diabetic rodent bone was structurally stronger than the non-diabetic rodent bone, but the higher peak force endured by the diaphysis during three-point (3pt) bending was not independent of the difference in body weight. Upon accounting for the structure of the femur diaphysis, the estimated toughness at 16weeks and 34weeks was lower for the diabetic mice than for non-diabetic controls, but neither toughness nor estimated material strength and resistance to crack growth (3pt bending of contralateral notched femur) decreased as the duration of hyperglycemia increased. With respect to trabecular bone, there were no differences in the compressive strength of the L6 vertebral strength between diabetic and non-diabetic mice at both ages despite a lower trabecular bone volume for the TallyHO than for the SWR/J mice at 34weeks. Amide I sub-peak ratios as determined by Raman Spectroscopy analysis of the femur diaphysis suggested a difference in collagen structure between diabetic and non-diabetic mice, although there was not a significant difference in matrix pentosidine between the groups. Overall, the fracture resistance of bone in the TallyHO model of T2D did not progressively decrease with increasing duration of hyperglycemia. However, given the variability in hyperglycemia in this model, there were correlations between blood glucose levels and certain structural properties including peak force.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  5 / 53429 MEDLINE  
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[PMID]: 29432813
[Au] Autor:Besio R; Iula G; Garibaldi N; Cipolla L; Sabbioneda S; Biggiogera M; Marini JC; Rossi A; Forlino A
[Ad] Address:Department of Molecular Medicine, Biochemistry Unit, University of Pavia, Pavia 27100, Italy. Electronic address: roberta.besio@unipv.it.
[Ti] Title:4-PBA ameliorates cellular homeostasis in fibroblasts from osteogenesis imperfecta patients by enhancing autophagy and stimulating protein secretion.
[So] Source:Biochim Biophys Acta;1864(5 Pt A):1642-1652, 2018 Feb 10.
[Is] ISSN:0006-3002
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:The clinical phenotype in osteogenesis imperfecta (OI) is attributed to the dominant negative function of mutant type I collagen molecules in the extracellular matrix, by altering its structure and function. Intracellular retention of mutant collagen has also been reported, but its effect on cellular homeostasis is less characterized. Using OI patient fibroblasts carrying mutations in the α1(I) and α2(I) chains we demonstrate that retained collagen molecules are responsible for endoplasmic reticulum (ER) enlargement and activation of the unfolded protein response (UPR) mainly through the eukaryotic translation initiation factor 2 alpha kinase 3 (PERK) branch. Cells carrying α1(I) mutations upregulate autophagy, while cells with α2(I) mutations only occasionally activate the autodegradative response. Despite the autophagy activation to face stress conditions, apoptosis occurs in all mutant fibroblasts. To reduce cellular stress, mutant fibroblasts were treated with the FDA-approved chemical chaperone 4-phenylbutyric acid. The drug rescues cell death by modulating UPR activation thanks to both its chaperone and histone deacetylase inhibitor abilities. As chaperone it increases general cellular protein secretion in all patients' cells as well as collagen secretion in cells with the most C-terminal mutation. As histone deacetylase inhibitor it enhances the expression of the autophagic gene Atg5 with a consequent stimulation of autophagy. These results demonstrate that the cellular response to ER stress can be a relevant target to ameliorate OI cell homeostasis.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  6 / 53429 MEDLINE  
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[PMID]: 29408699
[Au] Autor:Thomas CJ; Cleland TP; Sroga GE; Vashishth D
[Ad] Address:Department of Biomedical Engineering, Rensselaer Polytechnic Institute, Troy, NY 12182, USA; Center for Biotechnology and Interdisciplinary Studies, Rensselaer Polytechnic Institute, Troy, NY 12182, USA.
[Ti] Title:Accumulation of carboxymethyl-lysine (CML) in human cortical bone.
[So] Source:Bone;110:128-133, 2018 Feb 02.
[Is] ISSN:1873-2763
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Advanced glycation end-products (AGEs) are a category of post translational modification associated with the degradation of the structural properties of multiple different types of tissues. Typically, AGEs are the result of a series of post-translational modification reactions between sugars and proteins through a process known as non-enzymatic glycation (NEG). Increases in the rate of NEG of bone tissue are associated with type 2 diabetes and skeletal fragility. Current methods of assessing NEG and its impact on bone fracture risk involve measurement of pentosidine or total fluorescent AGEs (fAGEs). However, pentosidine represents only a small fraction of possible fAGEs present in bone, and neither pentosidine nor total fAGE measurement accounts for non-fluorescent AGEs, which are known to form in significant amounts in skin and other collagenous tissues. Carboxymethyl-lysine (CML) is a non-fluorescent AGE that is often measured and has been shown to accumulate in tissues such as skin, heart, arteries, and intervertebral disks, but is currently not assessed in bone. Here we show the localization of CML to collagen I using mass spectrometry for the first time in human bone. We then present a new method using demineralization followed by heating and trypsin digestion to measure CML content in human bone and demonstrate that CML in bone is 40-100 times greater than pentosidine (the current most commonly used marker of AGEs in bone). We then establish the viability of CML as a measurable AGE in bone by showing that levels of CML, obtained from bone using this technique, increase with age (p<0.05) and are correlated with previously reported measures of bone toughness. Thus, CML is a viable non-fluorescent AGE target to assess AGE accumulation and fragility in bone. The method developed here to extract and measure CML from human bone could facilitate the development of a new diagnostic assay to evaluate fracture risk and potentially lead to new therapeutic approaches to address bone fragility.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  7 / 53429 MEDLINE  
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[PMID]: 29523921
[Au] Autor:Kido T; Hoashi T; Kitano M; Shimada M; Kurosaki K; Ishibashi-Ueda H; Ichikawa H
[Ad] Address:Department of Pediatric Cardiovascular Surgery, National Cardiovascular and Cerebral Center, 5-7-1, Fujishiro-dai, Suita, Osaka, 565-8565, Japan.
[Ti] Title:Impact of Hybrid Stage 1 Palliation for Hypoplastic Left Heart Syndrome: Histopathological Findings.
[So] Source:Pediatr Cardiol;, 2018 Mar 09.
[Is] ISSN:1432-1971
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:The purpose of the study is to analyze the impact of hybrid stage 1 palliation on right ventricular myocardial pathology in hypoplastic left heart syndrome. Sufficient amount of right ventricular biopsies could be obtained from 16 of 32 patients who underwent Norwood operation between 2007 and 2013. Histopathological findings of right ventricle in patients who underwent primary Norwood operation (primary group, n = 5), patients with aortic atresia (HS1P AA group, n = 6) or aortic stenosis (HS1P AS group, n = 5) who underwent staged Norwood palliation following hybrid stage 1 palliation were compared. To eliminate the influence of right ventricular pressure afterload, right ventricular biopsies were obtained from patients with truncus arteriosus communis (TAC group, n = 6) at total correction. The percentage of myocardial fibrosis was significantly higher in both HS1P groups than in TAC group; moreover, it was significantly higher in HS1P AA group than in primary group. Capillary vascular density was significantly lower in all hypoplastic left heart syndrome groups than in TAC group. At the sub-endocardial layer, collagen type I/III ratios were higher in HS1P AA group than in other hypoplastic left heart syndrome groups. The proportions of N-cadherin immunolocalized to myocyte termini were lower in all hypoplastic left heart syndrome groups than in TAC group. Right ventricle in hypoplastic left heart syndrome showed more significant ischemic change and myocardial immaturity than that in truncus arteriosus communis. Hybrid stage 1 palliation for aortic atresia would be a risk factor for further right ventricular myocardial ischemia.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher
[do] DOI:10.1007/s00246-018-1851-6

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[PMID]: 29522822
[Au] Autor:Rasheeda K; Bharathy H; Nishad Fathima N
[Ad] Address:Inorganic and Physical Chemistry Laboratory, CSIR-Central Leather Research Institute, Adyar, Chennai 600020, India.
[Ti] Title:Vanillic acid and syringic acid: Exceptionally robust aromatic moieties for inhibiting in vitro self-assembly of type I collagen.
[So] Source:Int J Biol Macromol;, 2018 Mar 06.
[Is] ISSN:1879-0003
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:Excess collagen fibril accumulation is one of the leading causes for stroke and myocardial infarction, thus inducing interest in identifying and studying the compounds, which inhibits collagen fibril formation. Herein, inhibition of self-assembly of collagen has been studied using syringic acid and vanillic acid. These plant phytochemicals are well known antioxidants and they reduce oxidative stress as well. Inhibitory effect on collagen fibrils using syringic and vanillic acid has been studied using varying biophysical techniques. Circular Dichroism and FT-IR studies clearly showed the changes in secondary structure of collagen with the increasing concentration of vanillic acid and syringic acid. DLS measurements showed an acute aggregation upon treatment with these compounds and an inhibitory effect was also visualized using morphological studies. In addition, the decreased rate in the formation of collagen fibrils proves that these compounds are efficient to inhibit collagen fibril formation. This opens a new arena for the development of novel targeted delivery systems for diseases related to collagen accumulation.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:Publisher

  9 / 53429 MEDLINE  
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[PMID]: 29496505
[Au] Autor:Lee A; Karamichos D; Onochie OE; Hutcheon AEK; Rich CB; Zieske JD; Trinkaus-Randall V
[Ad] Address:Department of Biochemistry, Boston University School of Medicine, 80 E. Concord St., Boston, MA, 02118, USA. Electronic address: rusna9632@gmail.com.
[Ti] Title:Hypoxia modulates the development of a corneal stromal matrix model.
[So] Source:Exp Eye Res;170:127-137, 2018 Feb 27.
[Is] ISSN:1096-0007
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Deposition of matrix proteins during development and repair is critical to the transparency of the cornea. While many cells respond to a hypoxic state that can occur in a tumor, the cornea is exposed to hypoxia during development prior to eyelid opening and during the diurnal sleep cycle where oxygen levels can drop from 21% to 8%. In this study, we used 2 three-dimensional (3-D) models to examine how stromal cells respond to periods of acute hypoxic states. The first model, a stromal construct model, is a 3-D stroma-like construct that consists of human corneal fibroblasts (HCFs) stimulated by a stable form of ascorbate for 1, 2, and 4 weeks to self-assemble their own extracellular matrix. The second model, a corneal organ culture model, is a corneal wound-healing model, which consists of wounded adult rat corneas that were removed and placed in culture to heal. Both models were exposed to either normoxic or hypoxic conditions for varying time periods, and the expression and/or localization of matrix proteins was assessed. No significant changes were detected in Type V collagen, which is associated with Type I collagen fibrils; however, significant changes were detected in the expression of both the small leucine-rich repeating proteoglycans and the larger heparan sulfate proteoglycan, perlecan. Also, hypoxia decreased both the number of Cuprolinic blue-positive glycosaminoglycan chains along collagen fibrils and Sulfatase 1, which modulates the effect of heparan sulfate by removing the 6-O-sulfate groups. In the stromal construct model, alterations were seen in fibronectin, similar to those that occur in development and after injury. These changes in fibronectin after injury were accompanied by changes in proteoglycans. Together these findings indicate that acute hypoxic changes alter the physiology of the cornea, and these models will allow us to manipulate the conditions in the extracellular environment in order to study corneal development and trauma.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:Publisher

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[PMID]: 29458048
[Au] Autor:Park HJ; Son HJ; Sul OJ; Suh JH; Choi HS
[Ad] Address:Department of Biological Sciences, University of Ulsan, Ulsan 680-749, Republic of Korea.
[Ti] Title:4-Phenylbutyric acid protects against lipopolysaccharide-induced bone loss by modulating autophagy in osteoclasts.
[So] Source:Biochem Pharmacol;151:9-17, 2018 Feb 16.
[Is] ISSN:1873-2968
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:4-Phenylbutyric acid (4-PBA) has been used clinically to treat urea cycle disorders and is known to be an inhibitor of endoplasmic reticulum (ER) stress. We hypothesized that 4-PBA attenuates inflammatory bone loss by inducing autophagy, a process that is frequently accompanied by ER stress. Micro computerized tomography analysis showed that 4-PBA attenuated LPS-induced bone loss in mice. The increased area of TRAP-positive osteoclasts (OCs) and serum level of collagen type I fragments in lipopolysaccharide (LPS)-treated mice were also decreased when 4-PBA was administered, suggesting a protective role of 4-PBA in OCs. In vitro, 4-PBA significantly reduced OC area without affecting the number of OCs induced by LPS and decreased bone resorption upon LPS stimulation. LPS-induced autophagy was attenuated by 4-PBA in OCs, as demonstrated by reduced LC3II accumulation, increased p62 level, and reduction in AVO-containing cells. Silencing of autophagy-related protein 7 attenuated the effects of 4-PBA on OC size and fusion. Moreover, 4-PBA reduced nuclear factor-κB (NF-κB) DNA binding upon LPS stimulation of OCs. Inhibition of NF-κB activation diminished the inhibitory effect of 4-PBA on LPS-stimulated changes in LC3II level, OC area, and OC fusion, implying that the effects of 4-PBA on OCs are due at least in part to inhibition of NF-κB. These data demonstrate that 4-PBA attenuates LPS-induced bone loss by reducing autophagy in OCs. Our data highlight the therapeutic potential of 4-PBA for ameliorating inflammatory bone loss.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:Publisher


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